Cancer is often thought of as a disease of aging. Older people are at higher risk because cell damage that can lead to tumor formation has had more time to accumulate. But with cancer rates rising among young adults, and each generation facing a higher risk than the previous one, researchers wonder if cell damage is accumulating faster in recent generations, accelerating the body’s biological aging.
A new study led by researchers at Washington University School of Medicine in St. Louis provides evidence that younger generations are actually aging biologically faster than older generations. The cause is still being investigated around the world, including in a global effort by researchers at the Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine, and by Cancer Grand Challenge, a global initiative co-founded by the National Cancer Institute and Cancer Research UK. But importantly, new research shows that this accelerated aging is associated with an increased risk of early cancer development in younger people. Early-onset cancer generally refers to cancer that is diagnosed before age 55.
According to researchers, the greater the gap between biological age (what our bodies look like) and chronological age (how many years we actually live), the higher the risk of cancer. They found that people in newer birth cohorts had larger age differences than people in older birth cohorts. This may help explain the increase in early-onset cancer in recent generations.
Their study also identified a link between accelerated aging in certain organ systems and increased risk of certain cancers. For example, an immune system that looks older than its actual age was associated with earlier-onset lung cancer. Similarly, adipose tissue that appeared older than its chronological age was associated with earlier-onset colorectal cancer.
The study, published June 22 in the journal Nature Medicine, suggests that measuring accelerated aging may help identify individuals at high risk of developing early cancer and guide new strategies for cancer prevention and early detection.
Our ultimate goal is to decipher how the modern environment is biologically hardwired to promote cancer risk, moving prevention from broad recommendations to individualized interventions. This allows for early identification of risks and the development of preventive strategies tailored to individual biology. ”
Dr. Ying Kao, molecular epidemiologist and associate professor of surgery and medicine at WashU Medicine
Exploring biological aging
Cao’s team has been at the forefront of identifying individual factors that influence cancer risk across the life course, including obesity, metabolic dysregulation, alcohol consumption, sedentary behavior, poor diet, and caesarean section. These findings have revealed important clues about the origins of cancer in young people, but the contribution of any single factor is small.
With that in mind, Cao, also a member of the Siteman research team, and his colleagues have been looking for ways to capture the effects of multiple risk factors that work together to promote cancer development. With support from Cancer Grand Challenges, Cao was able to tackle this problem as co-leader of team PROSPECT.
For the current study, Professor Cao’s team analyzed data from more than 154,000 young people in the UK Biobank, a large-scale biomedical dataset that includes biological, health, and lifestyle data, as well as data from more than 10,000 individuals in the United States participating in the National Institute for Health Research’s (NIH) All of Us Research program, an initiative to build a comprehensive health dataset of more than 1 million people living in the United States.
To estimate the level of biological aging, or age differences, the researchers, including lead author Ruiyi Tian, a doctoral student in Cao’s lab, examined aging at two levels: aging throughout the body, known as systemic aging, and aging within individual organs, known as organ-specific aging. For systemic aging, the researchers used established measures, including clinical biomarker-based measures such as PhenoAge and the Klemera-Doubal method, as well as metabolomic age scores, which provide a measure of an individual’s metabolism.
For example, PhenoAge measures nine blood biochemical markers, including albumin, which is made by the liver, and creatinine, a waste product that is removed by the kidneys. For organ-specific aging, researchers used blood proteomics data, which measures the levels of multiple proteins associated with specific organ systems, to estimate the biological aging of individual organs.
The researchers calculated the average age difference for each birth cohort and used the standard deviation to describe how different each group was from the study average. Standard deviation is a measure of how spread out the data points are around the mean.
The researchers found that in the UK, when chronological age was taken into account, people born between 1965 and 1974 had a 23% increase in overall aging compared with those born between 1950 and 1954. In other words, for the same chronological age, people in younger birth cohorts showed smaller changes to older biological profiles than people in older birth cohorts.
Researchers observed a similar pattern in the U.S. cohort. Participants born between 1990 and 1999 had 92% one standard deviation higher overall aging compared with participants born between 1965 and 1969.
This increase in systemic aging in young people was associated with an 8% increased risk of early-onset solid cancers, particularly lung, gastrointestinal, and uterine cancers. When participants were divided into three groups based on their level of systemic aging, the group with the most advanced systemic aging had a 15% increased risk of early-onset solid cancer compared to the group with the least advanced systemic aging. The increased risk persisted even after controlling for genetic risk for cancer and genetic susceptibility to accelerated aging, according to the analysis.
By focusing on organ-specific aging, researchers found that progressive aging of the immune system was associated with an increased risk of early-onset lung cancer, and progressive aging of adipose (fat) tissue was associated with an increased risk of early-onset colorectal cancer.
“If we can identify young people who are most at risk for cancer when they are healthy, we can focus prevention and early detection strategies on those who would benefit most from early intervention,” Cao said.
The study is part of Team PROSPECT, a Cancer Grand Challenges team co-led by Cao. Cancer Grand Challenges is a global research funding initiative co-founded by Cancer Research UK and the National Cancer Institute (NCI), bringing together the world’s top researchers to tackle cancer’s toughest challenges.
“While we currently do not have definitive answers as to what is driving the rise in early-onset cancers around the world, studies like this help put the picture together and show that cancer can be influenced by broader changes occurring throughout the body, not just changes within individual cells,” said Dr. David Scott, Director of Cancer Grand Challenges. “Research on this scale is made possible through Cancer Grand Challenges, which bring together scientists from different fields around the world to work together on these complex problems.”
Cao and his colleagues are leading an effort to change our understanding of why cancer is on the rise among young people. Their next frontier is deciphering how environmental, lifestyle, and social changes leave lasting biological traces, such as accelerated aging and other markers of increased susceptibility. By uncovering the pathways by which risk accumulates across the life course, they seek to uncover the origins of early-onset cancer and redefine opportunities for prevention. At the same time, their research enables more precise approaches to identifying those most at risk and intervening earlier, shifting the paradigm from responding to disease to preventing disease before it begins.
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Reference magazines:
Tian, R. others. (2026) Biological aging and generational changes in early-onset cancer risk. natural medicine. DOI: 10.1038/s41591-026-04448-w. https://www.nature.com/articles/s41591-026-04448-w
